Search results for "2.1 Biological and endogenous factors"

showing 10 items of 53 documents

Genome-wide Analyses Identify KIF5A as a Novel ALS Gene

2018

© 2018 Elsevier Inc.

MaleAls geneGenome-wide association studyFAMILIAL ALSALS; axonal transport; cargo; GWAS; KIF5A; WES; WGS0302 clinical medicine80 and overPsychologyGWASKIF5AAetiologycargoAged 80 and over0303 health sciencesFrench ALS ConsortiumKinesinKINESIN HEAVY-CHAINCognitive Sciencesaxonal transportHumanHereditary spastic paraplegiaNeuroscience(all)Single-nucleotide polymorphismTARGETED DISRUPTIONArticle03 medical and health sciencesGeneticsHumansAmino Acid SequenceLoss functionAgedHEXANUCLEOTIDE REPEATNeuroscience (all)MUTATIONSAmyotrophic Lateral Sclerosis3112 Neurosciences1702 Cognitive Sciencemedicine.diseaseITALSGEN ConsortiumAnswer ALS Foundation030104 developmental biologyALS Sequencing ConsortiumHuman medicine1109 Neurosciences030217 neurology & neurosurgery0301 basic medicineALS; GWAS; KIF5A; WES; WGS; axonal transport; cargo[SDV]Life Sciences [q-bio]KinesinsNeurodegenerativeGenetic analysisGenomeAMYOTROPHIC-LATERAL-SCLEROSIS3124 Neurology and psychiatryCohort StudiesPathogenesisLoss of Function MutationMissense mutation2.1 Biological and endogenous factorsAmyotrophic lateral sclerosisNYGC ALS ConsortiumGeneticsGeneral NeuroscienceALS axonal transport cargo GWAS KIF5A WES WGSMiddle AgedPhenotypeSettore MED/26 - NEUROLOGIANeurologicalProject MinE ALS Sequencing ConsortiumKinesinWESFemaleAdultBiologyGENOTYPE IMPUTATIONALS; axonal transport; cargo; GWAS; KIF5A; WES; WGS; Adult; Aged; Aged 80 and over; Amino Acid Sequence; Amyotrophic Lateral Sclerosis; Cohort Studies; Female; Genome-Wide Association Study; Humans; Kinesin; Loss of Function Mutation; Male; Middle Aged; Young AdultNOYoung AdultRare DiseasesmedicineSLAGEN ConsortiumGene030304 developmental biologyClinical Research in ALS and Related Disorders for Therapeutic Development (CReATe) ConsortiumNeurology & NeurosurgeryHuman GenomeNeurosciencesAXONAL-TRANSPORTBrain DisordersALS; axonal transport; cargo; GWAS; KIF5A; WES; WGS;Family memberDNA-DAMAGEMOTOR-NEURONS3111 BiomedicineCohort StudieALSGenomic Translation for ALS Care (GTAC) ConsortiumWGSAmyotrophic Lateral SclerosiGenome-Wide Association StudyALS; axonal transport; cargo; GWAS; KIF5A; WES; WGS; Neuroscience (all)
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The genomic landscape of the Ewing Sarcoma family of tumors reveals recurrent STAG2 mutation.

2014

The Ewing sarcoma family of tumors (EFT) is a group of highly malignant small round blue cell tumors occurring in children and young adults. We report here the largest genomic survey to date of 101 EFT (65 tumors and 36 cell lines). Using a combination of whole genome sequencing and targeted sequencing approaches, we discover that EFT has a very low mutational burden (0.15 mutations/Mb) but frequent deleterious mutations in the cohesin complex subunit STAG2 (21.5% tumors, 44.4% cell lines), homozygous deletion of CDKN2A (13.8% and 50%) and mutations of TP53 (6.2% and 71.9%). We additionally note an increased prevalence of the BRCA2 K3326X polymorphism in EFT patient samples (7.3%) compared …

MaleCancer ResearchCell Cycle Proteinsmedicine.disease_causeFusion geneCDKN2AMedicine and Health Sciences2.1 Biological and endogenous factorsAetiologyChildGenetics (clinical)CancerPediatricMutationTissue microarrayTumorGenomeSarcomasHigh-Throughput Nucleotide SequencingAntigens NuclearSarcomaNeoplasm ProteinsOncologyChild PreschoolFemaleSarcomaResearch ArticleBiotechnologyHumanAdultPediatric Research Initiativelcsh:QH426-470Cohesin complexAdolescentPediatric CancerEwing SarcomaSarcoma EwingBiologyDisease-Free SurvivalFrameshift mutationCell LineGermline mutationRare DiseasesCell Line TumorEwingCancer GeneticsmedicineGeneticsHumansNuclearGenetic TestingAntigensPreschoolMolecular BiologyEcology Evolution Behavior and SystematicsGenome HumanHuman GenomeBiology and Life SciencesCancers and NeoplasmsInfantmedicine.diseaselcsh:GeneticsOrphan DrugMutationCancer researchGene DeletionDevelopmental Biology
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Global, regional, and national incidence, prevalence, and years lived with disability for 301 acute and chronic diseases and injuries in 188 countrie…

2015

Summary Background Up-to-date evidence about levels and trends in disease and injury incidence, prevalence, and years lived with disability (YLDs) is an essential input into global, regional, and national health policies. In the Global Burden of Disease Study 2013 (GBD 2013), we estimated these quantities for acute and chronic diseases and injuries for 188 countries between 1990 and 2013. Methods Estimates were calculated for disease and injury incidence, prevalence, and YLDs using GBD 2010 methods with some important refinements. Results for incidence of acute disorders and prevalence of chronic disorders are new additions to the analysis. Key improvements include expansion to the cause an…

MaleGerontologyNutrition and DiseaseEpidemiologyyears lived with disability Global burden of disease acute and chronic diseases countriesPrevalenceDiseaseGlobal HealthMedical and Health SciencesConduct disorderOtitis-mediaCost of IllnessResidence CharacteristicsVoeding en ZiekteEpidemiologyPrevalence80 and overGlobal health2.2 Factors relating to the physical environment2.1 Biological and endogenous factorscountriesAetiologyChildAged 80 and overMedicine(all)education.field_of_studyATTENTION-DEFICIT/HYPERACTIVITY DISORDERIncidenceMortality rateIncidence (epidemiology)Pain ResearchNeglected DiseasesAlcohol dependenceGeneral MedicineMiddle AgedGlobal burden of diseaseGlobal Burden of Disease Study 2013 CollaboratorsMental HealthInfectious DiseasesAttention deficit/Hyperactivity disorderBurden of IllnessChild PreschoolAcute DiseaseFemaleLife Sciences & BiomedicineAdultmedicine.medical_specialtyAdolescentGBD 2013Populationacute and chronic diseasesYoung AdultMental-disordersAge DistributionMedicine General & InternalWeightsGeneral & Internal MedicinemedicineHumansLife ScienceDisabled PersonsSex DistributionPreschooleducationDeveloping CountriesVLAGAgedScience & Technologybusiness.industryDeveloped CountriesCutaneous LeishmaniasisInfant NewbornInfantHealth outcomesNewbornmedicine.diseaseComorbidityBrain Disordersyears lived with disabilityGood Health and Well BeingDisease injury incidence prevalence YLDs GBD 2010Chronic DiseaseWounds and Injuriesbusiness2.4 Surveillance and distributionIron-deficiencyDemography
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Cross-species transcriptomic analysis elucidates constitutive aryl hydrocarbon receptor activity

2014

Background Research on the aryl hydrocarbon receptor (AHR) has largely focused on variations in toxic outcomes resulting from its activation by halogenated aromatic hydrocarbons. But the AHR also plays key roles in regulating pathways critical for development, and after decades of research the mechanisms underlying physiological regulation by the AHR remain poorly characterized. Previous studies identified several core genes that respond to xenobiotic AHR ligands across a broad range of species and tissues. However, only limited inferences have been made regarding its role in regulating constitutive gene activity, i.e. in the absence of exogenous ligands. To address this, we profiled transc…

MaleHEPATIC GENE-EXPRESSION413 Veterinary scienceMedical and Health SciencesTranscriptomeDIOXIN RECEPTORMice0302 clinical medicineTCDD-induced toxicityReceptorsTranscriptional regulationABNORMAL LIVER DEVELOPMENT2.1 Biological and endogenous factorsCluster AnalysisAetiologyReceptorAH RECEPTORIN-VIVOAryl hydrocarbon receptorGeneticsRegulation of gene expression0303 health sciencesBiological Sciencesrespiratory systemCore-gene batteryAryl HydrocarbonOrgan Specificity030220 oncology & carcinogenesisAHR endogenous ligands2378-TETRACHLORODIBENZO-P-DIOXIN TCDDSignal transductionResearch ArticleBiotechnologySignal TransductionProtein BindingBioinformatics1.1 Normal biological development and functioningeducationRAT-LIVERConstitutive gene expressionBiologyMICE LACKING03 medical and health sciencesSpecies SpecificityUnderpinning researchInformation and Computing SciencesGeneticsAnimals030304 developmental biologyAryl hydrocarbon receptor activityGene Expression ProfilingComputational BiologyAryl hydrocarbon receptorCELL-CYCLE CONTROLRatsrespiratory tract diseasesGene expression profilingReceptors Aryl HydrocarbonGene Expression RegulationSUBCHRONIC EXPOSUREbiology.proteinDigestive DiseasesTranscriptome
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Widening of the genetic and clinical spectrum of Lamb-Shaffer syndrome, a neurodevelopmental disorder due to SOX5 haploinsufficiency

2020

International audience; PURPOSE: Lamb-Shaffer syndrome (LAMSHF) is a neurodevelopmental disorder described in just over two dozen patients with heterozygous genetic alterations involving SOX5, a gene encoding a transcription factor regulating cell fate and differentiation in neurogenesis and other discrete developmental processes. The genetic alterations described so far are mainly microdeletions. The present study was aimed at increasing our understanding of LAMSHF, its clinical and genetic spectrum, and the pathophysiological mechanisms involved.METHODS: Clinical and genetic data were collected through GeneMatcher and clinical or genetic networks for 41 novel patients harboring various ty…

MaleMedizinHaploinsufficiencyL-SOX5VARIANTS0302 clinical medicineNeurodevelopmental disorderIntellectual disabilityMissense mutation2.1 Biological and endogenous factorsAetiologyChildGenetics (clinical)GeneticsPediatricGenetics & Heredity0303 health sciencesPedigreeFAMILYDNA-Binding Proteinsdevelopmental delayTRANSCRIPTION FACTORSPhenotypeintellectual disabilityChild Preschoolmissense variantsFemalemissense variants.HaploinsufficiencySOXD Transcription FactorsAdultEXPRESSIONAdolescentIntellectual and Developmental Disabilities (IDD)Clinical SciencesMutation MissenseautismCell fate determinationBiologyLONG FORMSEQUENCEArticle03 medical and health sciencesYoung AdultRare DiseasesClinical ResearchCARTILAGEIntellectual DisabilitymedicineGeneticsAnimalsHumansLanguage Development DisordersGenetic Predisposition to DiseasePreschoolTranscription factorGene030304 developmental biology[SDV.GEN]Life Sciences [q-bio]/GeneticsMUTATIONSHuman GenomeInfantmedicine.diseaseBrain DisordersNeurodevelopmental DisordersDeciphering Developmental Disorder StudyMutationAutismepilepsyMissense030217 neurology & neurosurgeryGENERATIONGenetics in Medicine
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Disruption of the ASTN2 / TRIM32 locus at 9q33.1 is a risk factor in males for Autism Spectrum Disorders, ADHD and other neurodevelopmental phenotypes

2014

Rare copy number variants (CNVs) disrupting ASTN2 or both ASTN2 and TRIM32 have been reported at 9q33.1 by genome-wide studies in a few individuals with neurodevelopmental disorders (NDDs). The vertebrate-specific astrotactins, ASTN2 and its paralog ASTN1, have key roles in glial-guided neuronal migration during brain development. To determine the prevalence of astrotactin mutations and delineate their associated phenotypic spectrum, we screened ASTN2/TRIM32 and ASTN1 (1q25.2) for exonic CNVs in clinical microarray data from 89 985 individuals across 10 sites, including 64 114 NDD subjects. In this clinical dataset, we identified 46 deletions and 12 duplications affecting ASTN2. Deletions o…

MaleReceptors Cell Surface/geneticsAutismChild Development Disorders Pervasive/geneticsGene ExpressionGenome-wide association studyMedical and Health SciencesTripartite Motif ProteinsRisk FactorsReceptors2.1 Biological and endogenous factorsProtein IsoformsNerve Tissue Proteins/geneticsCopy-number variationAetiologyChildGenetics (clinical)Sequence DeletionPediatricGenetics & HeredityGeneticseducation.field_of_studySingle NucleotideArticlesGeneral MedicineExonsBiological SciencesMental HealthPhenotypeAutism spectrum disorderOrgan SpecificityCerebellar cortexChild PreschoolCell SurfaceSpeech delayFemalemedicine.symptomTranscription Initiation SiteAttention Deficit Disorder with Hyperactivity/geneticsChromosomes Human Pair 9HumanPair 9AdultPediatric Research InitiativeChild Development DisordersAdolescentDNA Copy Number VariationsIntellectual and Developmental Disabilities (IDD)Ubiquitin-Protein LigasesPopulationTranscription Factors/geneticsNerve Tissue ProteinsReceptors Cell SurfaceBiologyPolymorphism Single NucleotideChromosomesYoung AdultClinical ResearchProtein Isoforms/geneticsBehavioral and Social ScienceGeneticsmedicineAttention deficit hyperactivity disorderHumansGenetic Predisposition to DiseasePolymorphismPreschooleducationMolecular BiologyGenetic Association StudiesPervasiveGlycoproteinsHuman GenomeNeurosciencesInfant NewbornGlycoproteins/geneticsInfantNewbornmedicine.diseaseBrain DisordersAttention Deficit Disorder with HyperactivityChild Development Disorders PervasiveCase-Control StudiesAutismTranscription Factors
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Exome sequencing in suspected monogenic dyslipidemias.

2015

Background— Exome sequencing is a promising tool for gene mapping in Mendelian disorders. We used this technique in an attempt to identify novel genes underlying monogenic dyslipidemias. Methods and Results— We performed exome sequencing on 213 selected family members from 41 kindreds with suspected Mendelian inheritance of extreme levels of low-density lipoprotein cholesterol (after candidate gene sequencing excluded known genetic causes for high low-density lipoprotein cholesterol families) or high-density lipoprotein cholesterol. We used standard analytic approaches to identify candidate variants and also assigned a polygenic score to each individual to account for their burden of commo…

MaleSettore MED/09 - Medicina InternaMedical BiotechnologyDNA sequencing; exome; exome sequencing; genetics human; lipids; mendelian geneticsBiologyCardiorespiratory Medicine and HaematologyNovel genelipidsmendelian geneticsGene mappingClinical ResearchGenetics2.1 Biological and endogenous factorsHumansgeneticsExomeDNA sequencinghumanAetiologyMendelian disordersExomeGenetics (clinical)Exome sequencingDyslipidemiasGeneticsInborn ErrorsHuman GenomeHigh-Throughput Nucleotide SequencingAtherosclerosisMetabolismCardiovascular System & Hematologylipids (amino acids peptides and proteins)DNA sequencing; exome; genetics; human; lipidsFemalegeneticCardiology and Cardiovascular Medicineexome sequencingexomeMetabolism Inborn ErrorsCirculation. Cardiovascular genetics
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Pan-cancer analysis of whole genomes

2020

Publisher's version (útgefin grein)

Maletert promoter mutationsCancer development and immune defence Radboud Institute for Molecular Life Sciences [Radboudumc 2]DNA Mutational AnalysisNormal tissuesystematic analysisGermlineTranscriptome0302 clinical medicineAetiologyCàncerCellular SenescenceCancer0303 health sciencesdna-damageMassive parallel sequencingPan cancerREARRANGEMENTSHigh-Throughput Nucleotide SequencingGenomicsSciences bio-médicales et agricolesTelomereCOMPREHENSIVE3. Good healthTERT PROMOTER MUTATIONSsignatures030220 oncology & carcinogenesisScience & Technology - Other TopicsErfðarannsóknirHuman:Informàtica::Aplicacions de la informàtica::Bioinformàtica [Àrees temàtiques de la UPC]EvolutionRNA SplicingGenomicsArticleEvolution MolecularStructural variationRC025403 medical and health sciencesSDG 3 - Good Health and Well-beingGeneticgenomicsSYSTEMATIC ANALYSISGeneticsGenomics--Databases.HumansGenetic TestingMolecular BiologySIGNATURESWhole genome sequencing1000 MultidisciplinaryChromothripsisScience & TechnologyRC0254 Neoplasms. Tumors. Oncology (including Cancer)Information DisseminationResearchInstitutes_Networks_Beacons/mcrcPreventionBiology and Life SciencesMolecularOncogenesCloud Computingmedicine.diseaseGenòmicaCompute cloudsMutation570 Life sciences; biologyCOMPREHENSIVE CHARACTERIZATIONGenèticaWhole Genome Sequencing--methodsBackground informationDNA Mutational Analysis ; Evolution ; Genetic / genetics ; Genome ; Genomics ; Germ-Line Mutation / genetics ; High-Throughput Nucleotide Sequencing ; Human / genetics ; Humans ; ICGC/TCGA Pan-Cancer Analysis of Whole Genomes ConsortiumMedizinGenomeWhole-genomeGenome mappingNeoplasms2.1 Biological and endogenous factorsPromoter Regions GeneticCàncer -- Aspectes genèticsTelomeraseGeneticsWomen's cancers Radboud Institute for Molecular Life Sciences [Radboudumc 17]MultidisciplinaryChromothripsisGenomeManchester Cancer Research Centregenomics cancer profiling3rd-DAS10124 Institute of Molecular Life SciencesWomen's cancers Radboud Institute for Health Sciences [Radboudumc 17]Multidisciplinary SciencesParallel sequencingICGC/TCGA Pan-Cancer Analysis of Whole Genomes ConsortiumFemaleprofilingMedical GeneticsEngineering sciences. TechnologyBiotechnologyGeneral Science & TechnologyThe Cancer Genome Atlas610 Medicine & healthComputational biologyQH426 GeneticsBiologyConsortium of the International Cancer Genome ConsortiumPromoter RegionsGermline mutationPan-cancer analysisKrabbameinsrannsóknirmedicinecancerddc:610QH426Germ-Line MutationMedicinsk genetikKrabbamein030304 developmental biologyCell ProliferationLANDSCAPEGenome Humancomprehensive characterizationPan-cancer analysis of whole genomesPoint mutationHuman GenomeCancerReproducibility of ResultsSOMATIC MUTATIONSEVOLUTIONCancer sequencing Chromothripsis telomereDNA-DAMAGEMutagenesisPATTERNS3111 BiomedicineCHARACTERIZATION
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Pancreatic T cell protein-tyrosine phosphatase deficiency ameliorates cerulein-induced acute pancreatitis.

2014

Background Acute pancreatitis (AP) is a common clinical problem whose incidence has been progressively increasing in recent years. Onset of the disease is trigged by intra-acinar cell activation of digestive enzyme zymogens that induce autodigestion, release of pro-inflammatory cytokines and acinar cell injury. T-cell protein tyrosine phosphatase (TCPTP) is implicated in inflammatory signaling but its significance in AP remains unclear. Results In this study we assessed the role of pancreatic TCPTP in cerulein-induced AP. TCPTP expression was increased at the protein and messenger RNA levels in the early phase of AP in mice and rats. To directly determine whether TCPTP may have a causal rol…

MessengerWistarProtein tyrosine phosphataseInbred C57BLBiochemistryOral and gastrointestinalSTAT3Mice2.1 Biological and endogenous factorsPhosphorylationAetiologySTAT3Non-Receptor Type 2CeruletideCancerMice KnockoutProtein Tyrosine Phosphatase Non-Receptor Type 2Pancreatitis Acute NecrotizingNF-kappa B3. Good healthAcute NecrotizingAmylasesTumor necrosis factor alphaTCPTPCell activationCeruletideSTAT3 Transcription Factormedicine.medical_specialtyBiochemistry & Molecular BiologyKnockoutBiologyProinflammatory cytokinePancreatic CancerRare DiseasesInternal medicineAcinar cellmedicineGeneticsAnimalsRNA MessengerRats WistarMolecular BiologyInflammationTumor Necrosis Factor-alphaInterleukin-6ResearchCell BiologyLipaseNFKB1RatsAcute pancreatitisMice Inbred C57BLEndocrinologyPancreatitisbiology.proteinRNAProtein Tyrosine PhosphataseBiochemistry and Cell BiologyDigestive DiseasesKnockout mice
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Missense variants in DPYSL5 cause a neurodevelopmental disorder with corpus callosum agenesis and cerebellar abnormalities

2021

International audience; The collapsin response mediator protein (CRMP) family proteins are intracellular mediators of neurotrophic factors regulating neurite structure/spine formation and are essential for dendrite patterning and directional axonal pathfinding during brain developmental processes. Among this family, CRMP5/DPYSL5 plays a significant role in neuronal migration, axonal guidance, dendrite outgrowth, and synapse formation by interacting with microtubules. Here, we report the identification of missense mutations in DPYSL5 in nine individuals with brain malformations, including corpus callosum agenesis and/or posterior fossa abnormalities, associated with variable degrees of intel…

Models MolecularMale0301 basic medicineHydrolases[SDV]Life Sciences [q-bio]Hippocampal formationMedical and Health Sciences0302 clinical medicineNeurodevelopmental disorderTubulinModelsNeurotrophic factorsCerebellumIntellectual disability2.1 Biological and endogenous factorsMissense mutationAetiologyChilddendrite branchingGenetics (clinical)de novo missense variantsPediatricGenetics & HeredityDPYSL5Biological Sciences[SDV] Life Sciences [q-bio]corpus callosum agenesisMental HealthChild PreschoolNeurologicalFemaleMicrotubule-Associated ProteinsAdultNeuriteIntellectual and Developmental Disabilities (IDD)primary neuronal culturesMutation MissenseBiologyYoung Adult03 medical and health sciencesRare DiseasesMediatorReportIntellectual DisabilityGeneticsmedicineHumansPreschoolCorpus Callosum Agenesisbrain malformationNeurosciencesMolecularmedicine.diseaseneurodevelopmental disorderBrain Disorders030104 developmental biologyNeurodevelopmental DisordersMutationMissenseAgenesis of Corpus CallosumNeuroscience030217 neurology & neurosurgery
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